Atox1 Drives Hepatocellular Carcinoma Progression Through C-myb And Pi3k/akt Activation

Background and aims

Despite advancements successful diagnostic and therapeutic strategies, hepatocellular carcinoma (HCC) remains a starring origin of cancer-related mortality. Antioxidant-1 (ATOX1) has been implicated successful oncogenic processes crossed various crab types; however, its circumstantial domiciled successful HCC remains unclear. This study aimed to analyse nan usability of ATOX1 and its underlying molecular mechanisms successful HCC.

Methods

Immunohistochemical study was conducted to measure ATOX1 look successful HCC tissues. Cell Counting Kit-8, colony formation, Transwell migration, travel cytometry, and reactive oxygen type (ROS) assays were employed to measure nan malignant behaviors of tumor cells. A xenograft rodent exemplary was employed to measure nan effects of ATOX1 knockdown connected tumor growth in vivo. DCAC50 curen was performed to inhibit nan copper carrier usability of ATOX1. RNA sequencing was conducted to research nan imaginable molecular mechanisms of ATOX1 successful HCC.

Results

ATOX1 look was importantly elevated successful HCC tumor tissues. ATOX1 promoted compartment proliferation, colony formation, and migration. Knockdown of ATOX1 suppressed tumor growth in vivo. Mechanistically, ATOX1 activated c-Myb, and frankincense enhanced nan malignant phenotype of HCC cells via activation of nan PI3K/AKT signaling pathway. Additionally, ATOX1 reduced intracellular copper accumulation and inhibited ROS accumulation and apoptosis. Inhibition of ATOX1 by DCAC50 decreased compartment proliferation while expanding ROS levels and apoptosis successful HCC cells. Notably, acetylcysteine reversed nan simplification successful c-Myb look induced by ATOX1 knockdown.

Conclusions

This study elucidates that ATOX1 promotes HCC carcinogenicity done nan c-Myb/PI3K/AKT signaling pathway while inhibiting copper accumulation, ROS generation, and apoptosis. These results bespeak that ATOX1 represents a imaginable therapeutic target for HCC. Moreover, nan compound DCAC50, by obstructing ATOX1's copper carrier function, efficaciously suppresses nan malignant behaviour of HCC cells, suggesting its promising domiciled successful HCC treatment, peculiarly erstwhile mixed pinch PI3K/AKT pathway inhibitors.